A 66-year-old woman with a history of atherosclerotic heart disease, adult onset diabetes mellitus and hypertension presented for a scheduled follow-up visit. She gave a history of rare episodes of stable exertional angina. Her therapeutic regimen included glyburide, hydrochlorothiazide, low salt, calorie restricted ADA diet and sublingual nitrates. During the preceding three months she required nitrates sporadically. Nonetheless, on certain occasions, predominantly during the morning hours, two nitroglycerin tablets were necessary to relieve her painful symptoms. No new or associated complaints were reported during these episodes. The last anginal attack occurred one week prior to her visit.
On physical examination she was normotensive with obvious changes of chronic osteoarthritis affecting knees and distal extremities. Cardiovascular findings included normal point of maximal impulse and heart sounds, a grade 1/6 systolic ejection murmur at the right sternal border, second intercostal space, consistent with aortic valve sclerosis. The carotid and peripheral pulses were normal. An electrocardiogram showed nonspecific ST-T abnormalities and was unchanged compared to previous tracings. A 24-hour ambulatory electrocardiographic recording showed frequent episodes of 2 mm ST segment depression predominantly in the morning hours. Therapy with long-acting beta blockers and topical nitrates resulted in excellent control of the angina. A repeat 24-hour ambulatory electrocardiographic recording revealed no evidence of ischemia.
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A 72-year-old white man with a history of chronic renal insufficiency and nephrotic syndrome secondary to idiopathic membranous glomerulopathy was brought to the emergency room with complaints of recurrent precordial pressure associated with mild shortness of breath. He had experienced three anginal episodes at rest and during usual activities at home in the early hours of the morning. During the last episode, the pain was more severe, prolonged and radiated to the left side of the neck and left shoulder. When he arrived at the emergency room four hours later, the symptoms had abated. He had no previous history of cardiac disease. Past medical history was otherwise remarkable for chronic obstructive pulmonary disease and gout. His current medications included theophylline SR, allopurinol, prednisone and furosemide.
Physical examination revealed blood pressure of 12(V75 mm Hg, pulse 86 beats/min, and respirations 20/min. Diffuse end-expiratory wheezes were heard over both lung fields. There was an St and S2 sound but no murmur could be heard. The carotid and jugular venous pulses were normal. An electrocardiogram revealed 2 mm ST segment elevation in leads V,-V3. Chest x-ray film revealed changes consistent with chronic obstructive pulmonary disease. Serum cholesterol level was 285 mg/dl; BUN, 45 mg/dl; creatinine, 2 mg/ dl. The patient received diltiazem, aspirin, oxygen and parenteral nitroglycerin. Serial electrocardiograms revealed transient T-wave inversion in V,-V3 followed by subsequent resolution of the injury pattern and reversion to a normal tracing 48 hours after admission. Serial creatinine kinase (CK) values were within the normal range; however, СКMВ band fraction reached maximal values of 11.2 percent during the first 24 hours. Ambulatory electrocardiographic monitoring (lead VjJ revealed episodes of painless ST elevation lasting 45 minutes. An echocardiogram revealed normal sized atrial and ventricular chambers, anteroseptal wall dyskinesia, and an ejection fraction of 50 percent. Cardiac catheterization performed on day 3 of hospitalization revealed 90 percent stenosis of the mid-left anterior descending coronary artery and anterior wall dyskinesia. There was no evidence of intracoronary thrombus. Subsequently, the patient underwent successful single vessel balloon angioplasty. tadacip 20 mg
4. Estimate the incidence of silent ischemia in the following subsets of patients with coronary artery disease: <10 percent; 10-20 percent; 20-30 percent; 40-50 percent; >50 percent